Western Association for Biofeedback and Neuroscience — Spring 2017 25 To speak of rigorous scientific thinking here is to exercise the imagination. This was a case of left-brained, top-down, mod- el-driven thinking run amok. The proof is now in hand. Of all the criticisms leveled at our clinical claims over the years, none has been borne out. This should be no sur- prise. Ours was a bottom-up process, and we never strayed far from the data. When we went public with a particular claim we had first-mover advantage, and that always wrong-footed the critics. In their accounting, every new claim just served to discredit us further. In our accounting, every instance just confirmed the folly of top-down regimentation of an emerging discipline in its most creative early phase. From the moment that Doug Quirk and Margaret Ayers got their hands on the in- strumentation for their clinical work, this has been a clinically driven field, with all that that implies. Almost all of the verities uttered by the arbiters of the field along the way have turned out to be wrong. I have just skimmed the surface. Ironically, the stunted thinking that has held sway over all these years also ex- tends to the theoretical underpinnings of neurofeedback, where the model-builders ought to be distinguishing themselves. It seems to have escaped notice that the op- erant conditioning model cannot possibly be the full explanation of neurofeedback. It cannot explain infra-low frequency training, for one thing, a problem that has now existed for ten years. But matters are much worse than that. It also could not explain the rapid results that were being obtained early on with SMR-be- ta training. Lubar even dismissed such claims on that account. ‘It is not possible to show results in less than fifteen ses- sions,’ he declared at the time. Either the rapid responses had to be discounted or the operant conditioning model had to be overhauled. Unsurprisingly, the data were discounted in order to leave the model intact. So the problem has existed for all these years, and yet was simply ignored even as the claim of quick results ceased to be controversial. Further, it doesn’t seem to bother any- one that the operant conditioning mod- el offers no insights into the supporting neurophysiology. It is a behavioral model. As essentially nothing more than a re-for- mulation of behavioral observations, it barely rises to the level of theory at all. In the words of physicist Jacob Bronowski, “..in the psychological sciences…the dis- tance between fact and theory…is small.” Neuroscientist J. Scott Kelso states the problem thus: “Often what passes for the- ory [in psychology] is a re-description of the facts, albeit in a different language.” Skinner was quite deliberate in his model formulation. Even as late as 1974 he asserted that “studying the brain is just another misguided quest to find the causes of behavior inside the organism rather than out in the world.” Given that mindset, the operant conditioning model is as far as you want to go, and as far as you can go. But two years earlier, in 1972, Sterman and Wyrwicka had published the first neurofeedback case study on epilep- sy in a human subject. An operant con- ditioning design had been used to affect brain behavior selectively and specifical- ly. Ironically, the boundary of Skinner’s black box had been breached with his own methods, but he missed the memo. Since the operant conditioning model cannot be stretched to cover the infra-low